Search results for "Chromosome instability"

showing 10 items of 38 documents

New chromosome numbers for plant taxa endemic to the Balearic Islands

2006

Mitotic chromosome numbers are reported from 25 vascular plant taxa, endemic to the Balearic Islands that are poorly known cytogenetically. The chromosome numbers ofAnthyllis vulneraria subsp.balearica (2n=12),Cymbalaria fragilis (2n=56), andPolygonum romanum subsp.balearicum (2n=40) were determined for the first time. A new chromosome number was found in several populations ofAnthyllis hystrix (2n=70) suggesting that this species is decaploid, in contrast to an earlier work reporting a higher ploidy level (2n=12x=84). The new chromosome number 2n=32 was reported inHypericum hircinum subsp.cambessedesii. It is suggested that the previous count (2n=40) could be explained by the presence of a…

GeneticsB chromosomeGenusChromosome instabilityPaleontologyChromosomeAnthyllisCymbalariaPlant SciencePloidyBiologybiology.organism_classificationHystrixFolia Geobotanica
researchProduct

Brief communication. Stable Drosophila buzzatii-Drosophila koepferae hybrids

1998

Previous experiments discovered high rates of chromosomal rearrangements in the progeny of males containing a telomeric segment of Drosophila koepferae in a D. buzzatii genetic background (segmental males). We have performed similar experiments, designed to test whether this chromosomal instability could be explained by a phenomenon similar to P-M hybrid dysgenesis or, alternatively, by a generalized telomeric effect. However, the results obtained have not allowed us to fully characterize this process, because we have not observed chromosomal rearrangements in the progeny of the putative unstable males. Our results suggest that chromosomal instability is independent of the introgressed frag…

GeneticsHigh rateDrosophila buzzatiiChromosome instabilityDrosophila koepferaeGeneticsBiologyMolecular BiologyGenetics (clinical)BiotechnologyHybridJournal of Heredity
researchProduct

The role of telomeres in predicting individual radiosensitivity of patients with cancer in the era of personalized radiotherapy.

2014

Radiotherapy plays a key role in cancer treatments, but tumor cell death differs from one tumor to another. The response of patients to radiotherapy varies considerably and adverse side effects are difficult to prevent. The mechanisms involved in the heterogeneity of this response are not well understood. In order to enhance the efficacy and safety of radiotherapy, it is important to identify subpopulations most at risk of developing a late adverse response to radiotherapy. Telomeres are composed of multiple repeats of a unique sequence of nucleotides forming a TTAGGG pattern. They protect chromosomes from end-to-end fusion and maintain genomic stability. Telomeres have been shown to be ext…

GeneticsTelomerasebusiness.industrymedicine.medical_treatmentCancerGeneral MedicineTelomeremedicine.diseaseRadiation ToleranceTelomereRadiation therapyTelomerase RNA componentOncologyMRN complexPredictive Value of TestsChromosome instabilityNeoplasmsmedicineCancer researchAnimalsHumansRadiology Nuclear Medicine and imagingTelomerase reverse transcriptasePrecision MedicinebusinessCancer treatment reviews
researchProduct

Fanconi anemia (FA) and crosslinker sensitivity: Re-appraising the origins of FA definition

2015

The commonly accepted definition of Fanconi anemia (FA) relying on DNA repair deficiency is submitted to a critical review starting from the early reports pointing to mitomycin C bioactivation and to the toxicity mechanisms of diepoxybutane and a group of nitrogen mustards causing DNA crosslinks in FA cells. A critical analysis of the literature prompts revisiting the FA phenotype and crosslinker sensitivity in terms of an oxidative stress (OS) background, redox-related anomalies of FA (FANC) proteins, and mitochondrial dysfunction. This re-appraisal of FA basic defect might lead to innovative approaches both in elucidating FA phenotypes and in clinical management.

Geneticsbusiness.industryDNA repairDNA damageMitomycin CDiepoxybutaneHematologymedicine.diseasemedicine.disease_causeFANC proteinschemistry.chemical_compoundOncologychemistryFanconi anemiaChromosome instabilityPediatrics Perinatology and Child HealthmedicineCancer researchbusinessOxidative stressPediatric Blood & Cancer
researchProduct

Simultaneous Aurora-A/STK15 overexpression and centrosome amplification induce chromosomal instability in tumour cells with a MIN phenotype

2007

Abstract Background Genetic instability is a hallmark of tumours and preneoplastic lesions. The predominant form of genome instability in human cancer is chromosome instability (CIN). CIN is characterized by chromosomal aberrations, gains or losses of whole chromosomes (aneuploidy), and it is often associated with centrosome amplification. Centrosomes control cell division by forming a bipolar mitotic spindle and play an essential role in the maintenance of chromosomal stability. However, whether centrosome amplification could directly cause aneuploidy is not fully established. Also, alterations in genes required for mitotic progression could be involved in CIN. A major candidate is represe…

Genome instabilityCancer ResearchCellular differentiationAneuploidyApoptosisCell CommunicationSpindle ApparatusBiologyProtein Serine-Threonine Kinaseslcsh:RC254-282Aurora KinasesChromosome instabilityChromosomal InstabilitymedicineTumor Cells CulturedGeneticsHumansRNA Small InterferingMitosisIn Situ Hybridization FluorescenceAurora Kinase ACentrosomePloidiesReverse Transcriptase Polymerase Chain ReactionAurora-A centrosomes amplification aneuploidyCell Differentiationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseAneuploidyCell biologySpindle apparatusUp-RegulationSettore BIO/18 - GeneticaCell Transformation NeoplasticPhenotypeMicroscopy FluorescenceOncologyCentrosomeColonic NeoplasmsEctopic expressionMicrosatellite InstabilityResearch ArticleBMC Cancer
researchProduct

CENPA overexpression promotes genome instability in pRb-depleted human cells

2009

Abstract Background Aneuploidy is a hallmark of most human cancers that arises as a consequence of chromosomal instability and it is frequently associated with centrosome amplification. Functional inactivation of the Retinoblastoma protein (pRb) has been indicated as a cause promoting chromosomal instability as well centrosome amplification. However, the underlying molecular mechanism still remains to be clarified. Results Here we show that pRb depletion both in wild type and p53 knockout HCT116 cells was associated with the presence of multipolar spindles, anaphase bridges, lagging chromosomes and micronuclei harbouring whole chromosomes. In addition aneuploidy caused by pRb acute loss was…

Genome instabilityCancer ResearchChromosomal Proteins Non-HistoneBlotting WesternBiologyAutoantigensRetinoblastoma Proteinlcsh:RC254-282Genomic InstabilityRNA interferenceChromosome instabilityCentromere Protein ACell Line TumorHumansRNA Processing Post-TranscriptionalDNA PrimersCENPABase SequenceReverse Transcriptase Polymerase Chain ReactionResearchRetinoblastoma proteincentromere protein aneuploidy pRBlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologyCell biologySettore BIO/18 - GeneticaSpindle checkpointOncologyMicroscopy FluorescenceCentrosomebiology.proteinMolecular MedicineRNA Interferencebiological phenomena cell phenomena and immunityCentromere Protein AMolecular Cancer
researchProduct

Bypass of cell cycle arrest induced by transient DNMT1 post-transcriptional silencing triggers aneuploidy in human cells

2012

Abstract Background Aneuploidy has been acknowledged as a major source of genomic instability in cancer, and it is often considered the result of chromosome segregation errors including those caused by defects in genes controlling the mitotic spindle assembly, centrosome duplication and cell-cycle checkpoints. Aneuploidy and chromosomal instability has been also correlated with epigenetic alteration, however the molecular basis of this correlation is poorly understood. Results To address the functional connection existing between epigenetic changes and aneuploidy, we used RNA-interference to silence the DNMT1 gene, encoding for a highly conserved member of the DNA methyl-transferases. DNMT1…

Genome instabilityCell cycle checkpointDNA damageAneuploidyBiologylcsh:RC254-282BiochemistryChromosome instabilitymedicineCentrosome duplicationEpigeneticsaneuploidylcsh:QH573-671Molecular BiologyGeneticsDNA methylationG1 arrestlcsh:CytologyResearchDNMT1Cell Biologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseCell biologySettore BIO/18 - GeneticaDNMT1 Aneuploidy epigenetic p14/ARF siRNADNA methylation
researchProduct

MAD2 depletion triggers premature cellular senescence in human primary fibroblasts by activating a P53 pathway preventing aneuploid cells propagation.

2012

The spindle assembly checkpoint (SAC) is a cellular surveillance mechanism that ensures faithful chromosome segregation during mitosis and its failure can result in aneuploidy. Previously, it was suggested that reduction of the MAD2 gene, encoding a major component of the SAC, induced aneuploidy in human tumor cells. However, tumor cell lines contain multiple mutations that might affect or exacerbate the cellular response to Mad2 depletion. Thus, the scenario resulting by Mad2 depletion in primary human cells could be different and more complex that the one depicted so far. We used primary human fibroblasts (IMR90) and epithelial breast cells (MCF10A) to gain further insight on the effects …

Genome instabilityCyclin-Dependent Kinase Inhibitor p21Cell cycle checkpointMad2PhysiologyClinical BiochemistryMAD2 depletion Aneuploidy Premature cellular senescence TP53Cell Cycle ProteinsBiologyCyclin-dependent kinaseChromosome instabilityChromosomal InstabilityTumor Suppressor Protein p14ARFHumansGene SilencingRNA Small InterferingMitosisCells CulturedCellular SenescenceCell ProliferationCalcium-Binding ProteinsCell BiologyCell Cycle CheckpointsFibroblastsAneuploidybeta-GalactosidaseCell biologyRepressor ProteinsSpindle checkpointSettore BIO/18 - GeneticaGene Expression RegulationMad2 Proteinsbiology.proteinM Phase Cell Cycle CheckpointsTumor Suppressor Protein p53Cell agingSignal Transduction
researchProduct

High resistance to X-rays and therapeutic carbon ions in glioblastoma cells bearing dysfunctional ATM associates with intrinsic chromosomal instabili…

2014

To investigate chromosomal instability and radiation response mechanisms in glioblastoma cells.We undertook a comparative analysis of two patient-derived glioblastoma cell lines. Their resistance to low and high linear energy transfer (LET) radiation was assessed using clonogenic survival assay and their intrinsic chromosome instability status using fluorescence in situ hybridization. DNA damage was analyzed by pulsed-field gel electrophoresis and by γ-H2AX foci quantification. Expression of DNA damage response proteins was assessed by immunoblot.Increased radioresistance to X-rays as well as carbon ions was observed in glioblastoma cells exhibiting high levels of naturally occurring chromo…

Genome instabilityDNA RepairDNA damageLinear energy transferHeavy Ion RadiotherapyAtaxia Telangiectasia Mutated ProteinsBiologyRadiation ToleranceCell Line TumorChromosomal InstabilityRadioresistanceChromosome instabilitymedicineHumansDNA Breaks Double-StrandedLinear Energy TransferRadiology Nuclear Medicine and imagingGel electrophoresisRadiological and Ultrasound Technologymedicine.diagnostic_testX-RaysCell CycleGenomicsMolecular biologyPhosphorylationGlioblastomaSignal TransductionFluorescence in situ hybridizationInternational Journal of Radiation Biology
researchProduct

Long-Lasting Genomic Instability Following Arsenite Exposure inMammalian Cells: The Role of Reactive Oxygen Species

2011

Previously, we reported that the progeny of mammalian cells, which has been exposed to sodium arsenite for two cell cycles, exhibited chromosomal instability and concurrent DNA hypomethylation, when they were subsequently investigated after two months of subculturing (about 120 cell generations) in arsenite-free medium. In this work, we continued our investigations of the long-lasting arsenite-induced genomic instability by analyzing additional endpoints at several time points during the cell expanded growth. In addition to the progressive increase of aneuploid cells, we also noted micronucleated and multinucleated cells that continued to accumulate up to the 50th cell generation, as well a…

Genome instabilitySodium arseniteEpidemiologyArsenitesHealth Toxicology and MutagenesisPopulationCellarsenite; genomic instability; reactive oxygen speciesCHO CellsBiologyGenomic Instabilitychemistry.chemical_compoundMultinucleateCricetulusChromosome instabilityCricetinaemedicineAnimalseducationGenetics (clinical)Arseniteeducation.field_of_studyCell cycleDNA MethylationFlow CytometryMolecular biologyarseniteSettore BIO/18 - Geneticamedicine.anatomical_structurechemistryEnvironmental PollutantsReactive Oxygen Species
researchProduct